Alzheimer's disease is cognitive disorder that denatures intracerebral nerve cells due to accumulating an amyloid β protein (hereinafter, abbreviated as “Aβ”) in the brain. For the pathogenesis, the most prevailing is the “amyloid hypothesis” such that soluble Aβ strongly inhibits long-term enhancement of memory and Aβ that is coagulated and deposited forms fibrils to thus lead nerve cells to death.
Due to administration of an antibody against Aβ (anti-Aβ antibody) and administration of an Aβ vaccine, deletion of Aβ deposition in the brain as well as improvement in symptoms of cognitive disorder were reported, and possibility that Alzheimer's disease can be treated was shown (Non-patent Document 1). However, administration of an Aβ vaccine caused death for side effects and a clinical trial was thus ceased (Non-patent Document 2); accordingly, the goal to establishing a therapeutic method for Alzheimer's disease is far. On the other hand, development of an anti-Aβ antibody excellent in therapeutic effects has progressed by a number of research groups, but a therapy with an anti-Aβ antibody is expensive and takes over a long period of time, and thus, burden on a patient is severe. In addition, an anti-Aβ antibody has a problem such that its effects are comparatively short, which thus requires repeated administrations. Note that Patent Documents 1 and 2 are shown as prior art documents.